Abstract
Background:
Lifetime risk for cardiovascular (CV) disease is high but predicting incident events on an individual level remains difficult. Single measurements of galectin-3, a marker of tissue fibrosis, predict mortality and new-onset heart failure (HF). Persistently elevated levels may indicate a clinically silent disease process.
Objectives:
Our aim was to establish the value of serial galectin-3 measurements to predict CV outcomes in the general population.
Methods:
Plasma galectin-3 was measured in the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) study at baseline and after ∼4 years. Changes in serial galectin-3 were expressed as categorical changes or absolute change from baseline and were related to subsequent outcome.
Results:
Serial galectin-3 was measured in 5958 subjects (mean age 49±12 years; 49% female). The median duration of follow-up was 8.3 years. Persistently elevated galectin-3 (defined as highest quartile at baseline and highest quartile during visit 2, n=757 subjects) was associated with a higher risk for new-onset HF, CV mortality, all-cause mortality, new-onset atrial fibrillation and CV events, compared with subjects with non-persistently elevated galectin-3. After multivariable adjustments for baseline characteristics, serial galectin-3 remained an independent predictor of new-onset HF (HR 1.85 (1.10-3.13); p=0.02) but not for other outcomes. Serial measurements provided more accurate prognostic value to predict new-onset HF, compared with a single baseline measurement (Harrell's C: 0.72 (0.68-0.75) vs 0.68 (0.65-0.72); p=0.002, respectively) with significant net reclassification.
Conclusions:
Persistently elevated galectin-3 predicts new-onset HF after adjustment for covariates, and serial measurements provide more accurate prognostic information compared with single determination of galectin-3. This may help to identify individuals who are at risk for incident HF and might provide a measure to monitor interventions.
Original language | English |
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Pages (from-to) | 1134-1141 |
Number of pages | 8 |
Journal | Heart |
Volume | 102 |
Issue number | 14 |
DOIs | |
Publication status | Published - 15 Jul 2016 |
Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2016 Published by the BMJ Publishing Group Limited. For permission to use.